SMAD2 and lung cancer: Additionally, CXCR7 function is subject to modulation by TGF-β signaling, as knockdown of CXCR7 has been shown to attenuate TGF-β1-induced migration, invasion, and epithelial-mesenchymal transition (EMT) in lung cancer cells (36), whereas CXCR7 overexpression enhances TGF-β1 secretion and promotes EMT through Smad2/3 phosphorylation in head and neck squamous cell carcinoma (37).